Background: The current prognosis of medulloblastoma in children is better because of technological advancements and improvements in treatment strategies and genetic investigations. However, there is a lack of studies that focus on medulloblastoma in Thailand. The aims of our study were to conduct a survival analysis and to identify the prognostic factors of pediatric medulloblastoma.
Materials And Methods: Fifty-five children, with medulloblastoma, were eligible for analysis between 1991 and 2015. We retrospectively reviewed both the clinical and the histological data. Survival curves were constructed using the Kaplan-Meier method. For comparisons of dichotomous factors, between groups, the log-rank test was used to determine survival. The Cox proportional hazard regression model was used to identify the univariate and multivariate survival predictors.
Results: The mortality rate was 49.1% in this study. The median follow-up time was 68.8 months (range: 1-294 months). The 5-year overall survival rate and median survival time were 53.8% (95% CI 38.7-66.7) and 80 months (95% CI 23-230), respectively. Univariate analysis revealed children <3 years of age, hemispheric tumor location, high risk according to risk stratification, and patients who did not receive radiation therapy affected the prognosis. In multivariable analysis, hemispheric tumors (hazard ratio [HR] 2.54 [95% CI 1.11-5.80]; = 0.01)and high risk groups (HR 3.86 [95% CI 1.28-11.60]; = 0.01) influenced death. Finally, using conditional inference trees, the study showed that hemispheric tumor locations are truly aggressive in behavior, whereas risk stratification is associated with the prognosis of midline tumors.
Conclusions: Hemispheric medulloblastoma and high-risk groups according to risk stratification were associated with poor prognosis.
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http://dx.doi.org/10.4103/jpn.JPN_111_17 | DOI Listing |
Pulmonology
December 2025
Department of General Surgery, Suzhou Ninth Hospital Affiliated to Soochow University, Suzhou, Jiangsu, China.
J Nephrol
January 2025
Department of Nephrology, Beaumont Hospital, Dublin, Ireland.
Background: Autosomal dominant polycystic kidney disease (ADPKD) is caused primarily by pathogenic variants in the PKD1 and PKD2 genes. Although the type of ADPKD variant can influence disease severity, rare, hypomorphic PKD1 variants have also been reported to modify disease severity or cause biallelic ADPKD. This study examines whether rare, additional, potentially protein-altering, non-pathogenic PKD1 variants contribute to ADPKD phenotypic outcomes.
View Article and Find Full Text PDFBiochem Genet
January 2025
Institute of Biological Sciences, Faculty of Science, Universiti Malaya, 50603, Kuala Lumpur, Malaysia.
Colorectal cancer (CRC) is the third most deadly cancer diagnosed in both men and women. 5-Fluorouracil (5-FU) treatment frequently causes the CRC cells to become chemoresistance, which has a negative impact on prognosis. Using bioinformatic techniques, this work describes important genes and biological pathways linked to 5-FU resistance in CRC cells.
View Article and Find Full Text PDFEsophagus
January 2025
Department of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Background: Herein, we aimed to examine the relationship between sarcopenia, neutrophil-lymphocyte ratio (NLR), Charlson comorbidity index (CCI), and prognostic nutritional index (PNI) in patients with superficial esophageal carcinoma who underwent definitive chemoradiotherapy (CRT).
Methods: We retrospectively analyzed 100 patients (87 males) diagnosed with cT1N0M0 esophageal squamous cell carcinoma. The included patients underwent CRT as an initial treatment.
Gastric Cancer
January 2025
Department of Biochemistry and Molecular Biology, Key Laboratory of Breast Cancer Prevention and Therapy, Ministry of Education, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China.
Background: Gastroesophageal junction adenocarcinoma (GEJAC) exhibits distinct molecular characteristics due to its unique anatomical location. We sought to investigate effective and reliable molecular classification of GEJAC to guide personalized treatment.
Methods: We analyzed the whole genomic, transcriptomic, T-cell receptor repertoires, and immunohistochemical data in 92 GEJAC patients and delineated the landscape of genetic and immune alterations.
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